INT275621

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Context Info
Confidence 0.06
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 2.15
Pain Relevance 0.04

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

transport (Atcay)
Anatomy Link Frequency
neuronal 1
platelet 1
astrocytes 1
Atcay (Mus musculus)
Pain Link Frequency Relevance Heat
Central nervous system 1 70.40 Quite High
Hippocampus 6 49.76 Quite Low
cytokine 25 33.12 Quite Low
Pyramidal cell 2 11.00 Low Low
Thalamus 27 5.00 Very Low Very Low Very Low
Inflammation 17 5.00 Very Low Very Low Very Low
corticosteroid 5 5.00 Very Low Very Low Very Low
chemokine 4 5.00 Very Low Very Low Very Low
lidocaine 3 5.00 Very Low Very Low Very Low
Action potential 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hypereosinophilic Syndrome 17 100.00 Very High Very High Very High
Creutzfeldt Jakob Disease 36 88.72 High High
Chronic Myeloid Leukemia 1 86.48 High High
Disease 44 86.20 High High
Celiac Disease 2 76.44 Quite High
Hypersensitivity 15 75.16 Quite High
Food Hypersensitivity 1 73.76 Quite High
Anaphylaxis 2 68.44 Quite High
Targeted Disruption 8 68.00 Quite High
Leukocytosis 1 51.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
NICD is translocated to neuronal nuclei where it activates the HES and HERP genes that inhibit the expression of pro-neuronal genes that maintain dendrites.
Positive_regulation (activates) of HES in neuronal
1) Confidence 0.06 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC2825502 Disease Relevance 0.28 Pain Relevance 0.04
Neuronal induction of hES cell-derived astrocytes
Positive_regulation (induction) of hES in astrocytes
2) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2708355 Disease Relevance 0 Pain Relevance 0
A subset of patients with HES have a 800 kb interstitial deletion on chromosome 4q12 that results in the fusion of a gene of unknown function, Fip1-like1 (FIP1L1), with the platelet-derived growth factor receptor-a (PDGFRA).74 Dysregulated tyrosine kinase activity by the FIP1L1-PDGFRA fusion gene has been identified as a cause of clonal HES, called FIP1L1-PDGFRA-positive CEL in humans.
Positive_regulation (cause) of HES in platelet associated with hypereosinophilic syndrome
3) Confidence 0.02 Published 2010 Journal Allergy, Asthma & Immunology Research Section Body Doc Link PMC2846745 Disease Relevance 1.87 Pain Relevance 0

General Comments

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